Issues

T cells show elevated markers of metabolic capacity in lung inflammation in vivo.

IL-17–producing T cells show the most pronounced expression of metabolic markers.

Glut1 and GLS inhibitors reduce cytokine production and enhance steroid therapy.

CTL33 maintains intestinal microbiota homeostasis in shrimp.

CTL33 mediates biofilm formation of intestinal bacteria.

CTL33 facilitates the establishment of intestinal bacteria in shrimp intestines.

Autoregulatory CD8 T cells contain a CXCR3⁺/IFN-γ⁺/IL-10⁺ subset.

CXCR3⁺ CNS-specific CD8 T cells can suppress EAE.

CagA suppressed expression of proinflammatory cytokines in vitro and in vivo.

CagA interacted with SHP-1 which facilitated the recruitment of SHP-1 to TRAF6.

CagA interacts with SHP-1 to inhibit the K63-linked polyubiquitination of TRAF6.

NK cells produce IL-10 during sepsis in an IL-15–dependent manner.

NK cell–derived IL-10 promotes host survival during sepsis.

NK cell–derived IL-10 is relevant to septic patients.

Functional analysis of Th1* immune signature genes uncovers novel regulators of IFN-γ and IL-17.

Loss of ISOC1 impairs CD4⁺ T cell pyrimidine metabolism, bioenergetics, and cytokine production.

IgG1 Fc peptides activate natural Treg, which regulate naive T cell differentiation.

Ag processing of the surface IgG on B cells activates Treg.

Fibrocytes enable CD8⁺ T cell activation mainly via CD86/CD28 costimulation.

Fibrocytes express functional PD-L1; PD-L1 blockade further activates CD8⁺ T cells.

Tumor-infiltrating fibrocytes have APC function enhanced by PD-1/PD-L1 blockade.

NK cells with unique receptor repertoires predominate at iNK, tNK, and mNK stages.

High interdependencies of NK cell receptor expression at the iNK stage were found.

In MHC-I–deficient mice, activating Ly-49 receptor expression is underrepresented.

The FATC domain is critical for ATM protein stability in vivo.

R3047X mutation in ATM FATC domain blocks lymphocyte development.

ATM-R3047X has compromised tumor suppression functions.

We developed Macaca mulatta (Mamu) CD1b-GMM and CD1c-GMM tetramers.

i.v. BCG leads to expansion of CD1c-GMM–specific T cells in the blood.

Some CD1c-GMM–specific T cells express a T_RM phenotype in BAL.

Semaphorin 3E protects against chlamydial lung infection.

Semaphorin 3E modulates DC and T cell function for effective immune response.

Vaccines were designed to induce only V1V2 Abs in NHP before SHIV challenge.

Vaccine-induced V2 Abs did not independently control SHIV infection.

Neutralizing and virus capture anti-Env Abs correlated with SHIV virus control.

Neutralizing Ab-opsonized HIV was cleared faster from blood circulation than HIV.

FcγRIIb, the lone FcγR expressed in human LSEC, clears Ab-HIV via endocytosis.

Endocytosed Ab-HIV localizes to lysosomes of LSEC.

Activation of TLR3⁺ moDCs predominates after respiratory viral infection.

TLR3 and moDCs are required for progressive postviral lung disease.

TLR3⁺ moDCs expand lung epithelial cells that are key to postviral disease.

Early-life RSV infection persistently alters the immune phenotype in BMDC.

TSLP has a role in the altered immune environment by inhibiting type 1 immunity.

RSV infection alters immune responses through epigenetic/transcriptional programs.

Tyrosine kinase inhibitors that target cAbl kinase inhibit inflammasome activation.

cAbl kinase deletion suppresses the ability to activate the NLRP3 inflammasome.

Tyrosine 146 of ASC is integral to speck formation and inflammasome function.

Teleost IFNφ1 was discovered as a broad powerful bactericidal cytokine.

IFNφ1 directly kills bacteria by cytoderm binding and disruption.

Potent antimicrobial peptide–like IFN-Is were identified in other gnathostomes.

SPM AT-RvD1 diminishes SHS-exacerbated, infection-induced pulmonary inflammation.

SHS-exposed mice demonstrated augmented antibacterial immunity when treated with AT-RvD1.

AT-RvD1–treated, SHS-exposed, vaccinated mice rapidly clear acute bacterial challenge.

An IFN gene signature is present in the inflamed mucosa of individuals with EoE.

This IFN signature is conserved between adults and children.

IFN-γ is produced by circulating EoE T cells activated with EoE-causal allergens.

Intratumoral T cells lose IFN-γ and GzmB and express elevated Tox and IL-10.

Agonistic αCD40 abrogates intratumoral IL-27, IL-10, and T_EX.

αCD40+αPD-L1 and abrogating Tnfrsf1a on host cells promotes tumor clearance.

CD155 is induced on macrophages in response to stimulation by IL-4 and LPS.

CD155 induction is dependent upon persistently active AhR.

CD155 can be targeted in vivo via AhR inhibition.

ASAH2 is overexpressed in MDSCs in human colon cancer patients.

The Slc5a11–GSH–GPX4–lipid ROS ferroptosis pathway is regulated by Asah2 in MDSCs.

Inhibition of Asah2 by NC06 suppresses MDSC accumulation in tumor-bearing mice.